Gallstone-related issues stand out as the most frequent trigger for acute pancreatitis (AP) on a global scale, a condition carrying significant risk. The precise mechanisms that lead to acute pancreatitis are still being researched. For accurate diagnosis and to predict how the condition might progress, laboratory tests and imaging are essential. Experts have proposed scoring systems that incorporate what’s seen in radiological scans along with blood markers of inflammation to better determine the severity of the disease. In certain cases of gallstone pancreatitis, early endoscopic retrograde cholangiopancreatography (ERCP) can be beneficial. The preferred treatment strategy for acute biliary pancreatitis involves laparoscopic cholecystectomy, often combined with endoscopic clearance of the common bile duct before surgery. However, the optimal timing for cholecystectomy after ERCP in cases of biliary pancreatitis can vary widely, depending on how severe the pancreatitis is.
Keywords: Biliary Pancreatitis Diagnosis, acute pancreatitis, gallstone pancreatitis, diagnosis, treatment, severity, ERCP, cholecystectomy
Gallstones are the primary culprit behind pancreatitis worldwide, responsible for at least half of all cases. In Western countries, this translates to a range of 4.8 to 24.2 pancreatitis cases per 100,000 individuals annually. In the United States alone, approximately 80,000 cases occur each year, equating to 17 new cases per 100,000 people. Japan reports an annual incidence between 5 and 80 cases per 100,000 population.
While most patients with biliary pancreatitis due to gallstones recover without lasting complications, a significant portion, between 15% and 30%, experience severe episodes. These severe cases necessitate complex, multidisciplinary care to optimize patient outcomes. Acute biliary pancreatitis can lead to both local complications, such as necrosis, pseudocyst formation, abscesses, and hemorrhage, and systemic complications, including pleural effusion, acute respiratory distress syndrome (ARDS), kidney dysfunction, and multiple organ failure. Managing these complex complications often requires intensive care unit (ICU) admission and specialized treatment.
Gender and the size of gallstones may play a role in the risk of gallstone pancreatitis. Men are statistically more likely to develop acute pancreatitis if they have gallstones. However, because gallstones are more common in women, more women ultimately develop gallstone pancreatitis overall.
Acute pancreatitis is a serious, potentially fatal disease with an overall mortality rate of 2% to 7%, despite advancements in medical interventions. The outcome of acute pancreatitis is largely determined by two key factors that reflect the disease’s severity: the presence of organ failure and pancreatic necrosis. Alarmingly, about half of all deaths from acute pancreatitis occur within the first one to two weeks, primarily due to multiple organ dysfunction syndromes. If left untreated, gallstone pancreatitis has a high recurrence rate, ranging from 32% to 61%.
UNDERSTANDING THE CAUSES OF ACUTE PANCREATITIS
The precise mechanisms that trigger acute pancreatitis are not yet fully understood. Specifically, how gallstones lead to pancreatitis remains unclear. One leading theory suggests that the reflux of bile into the pancreatic duct, caused by temporary blockage of the ampulla of Vater as gallstones pass through, is a key initiating event. For decades, there has been considerable interest in the early removal of any retained common bile duct (CBD) stones and the potential benefits for patients with acute biliary pancreatitis. Interestingly, later research revealed that over 85% of patients diagnosed with gallstone pancreatitis spontaneously pass the stones, which can be recovered in their stool.
This finding lends support to the ‘common channel theory,’ which posits a shared pathway for the bile and pancreatic ducts at the ampulla of Vater. However, further studies demonstrated that sterile bile alone does not cause pancreatitis. In contrast, infected bile has been shown to activate pancreatic enzymes, leading to the pancreas digesting itself, a process known as autodigestion. Two main concepts are currently favored as explanations for the onset of gallstone pancreatitis: (a) the reflux of infected bile into the pancreas, triggering a cascade of digestive enzyme activation, and (b) obstruction of the pancreatic duct, resulting in acinar disruption due to increased pressure. A potentially unifying hypothesis, proposed by Moody in 1993, suggests that gallstones initiate pancreatitis by obstructing the pancreatic duct, and the progression to necrosis and severe pancreatitis requires the reflux of bile.
Experimental models have further shown that zymogen granules, which contain inactive digestive enzymes, merge with lysosome vacuoles within pancreatic cells. This fusion leads to the activation of proteolytic enzymes within the pancreas itself. Small amounts of trypsin, a key digestive enzyme, can be neutralized by the body’s natural pancreatic trypsin inhibitor. However, when large amounts of trypsin are released, the body’s defense mechanisms, such as α-1-antitrypsin and α-2-macroglobulin, can be overwhelmed. This enzymatic overload then activates other enzymes, setting off a chain reaction that leads to the local and systemic complications commonly seen in acute pancreatitis. The activation of phospholipase A2, another enzyme, has significant consequences, including the destruction of pulmonary surfactant, which can result in ARDS. Furthermore, the release of prostaglandins and leukotrienes plays a crucial role in the systemic inflammatory response, potentially leading to multi-organ failure. These inflammatory mediators are increasingly being explored as potential markers to predict the severity of the disease in the near future. Trypsin also activates kinin and kallikrein systems, possibly contributing to disseminated intravascular coagulation, shock, kidney failure, and vascular instability.
DIFFERENTIATING BILIARY PANCREATITIS FROM OTHER TYPES: THE DIAGNOSTIC PROCESS
When diagnosing biliary pancreatitis, a history of biliary colic should raise suspicion. While gallstone pancreatitis is the most frequent cause, it’s essential to consider other potential causes before starting treatment. These include excessive alcohol consumption over time, medications, genetic disorders, infections, post-surgical conditions, endoscopic procedures involving the pancreatic and bile ducts, and other forms of pancreatic injury. A thorough patient history and a detailed physical examination are the initial critical steps in establishing an accurate diagnosis of biliary pancreatitis. Following these initial steps, laboratory and radiological investigations become crucial, not only for confirming the diagnosis but also for predicting the prognosis of a patient presenting with suspected gallstone pancreatitis. Documenting elevated serum amylase and/or lipase levels is a standard diagnostic practice for pancreatitis. Serum amylase is elevated in at least 75% of acute pancreatitis cases and typically remains elevated for 5 to 10 days. However, amylase is not specific to pancreatitis as it can be elevated in other conditions. Lipase is more specific for pancreatitis, but both enzymes can be elevated in cases of kidney failure and various abdominal conditions such as perforated ulcers, mesenteric vascular occlusion, and intestinal obstruction. Other reasons for increased serum amylase include salivary gland issues, macroamylasemia (amylase bound to proteins in the blood), and tumors that secrete amylase. Serum lipase has a longer half-life than amylase, meaning it tends to stay elevated for a longer period. Using a cutoff value of three times the upper limit of normal, the sensitivity of serum lipase in diagnosing pancreatitis in patients presenting with abdominal pain approaches 90%. A urine dipstick test for trypsinogen-2 has demonstrated a sensitivity and specificity exceeding 90% for acute pancreatitis and can be a rapid point-of-care diagnostic tool.
Several blood tests can aid in distinguishing biliary pancreatitis from pancreatitis caused by other factors. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase, and serum bilirubin, collectively known as liver function tests, are important to assess when diagnosing biliary pancreatitis.
A recent study highlighted the specificity of a serum ALT level exceeding 150 IU/L for diagnosing gallstone pancreatitis, reaching 96%. However, the sensitivity was only 48%. This implies that while a high ALT level in the appropriate clinical context strongly suggests biliary pancreatitis, a normal ALT level does not rule out gallstones as the cause. Researchers are actively exploring experimental biochemical markers to better assess disease severity, including trypsinogen activation peptide, interleukin-6, interleukin-10, procalcitonin, phospholipase A2, and C-reactive protein levels. Currently, the clinical availability of these markers is limited, but there is significant interest in understanding immune response markers and pancreatic injury markers. These could become valuable tools for reliably predicting the severity of acute pancreatitis and complementing imaging techniques in the diagnostic process.
Imaging plays a vital role in confirming the diagnosis of biliary pancreatitis and assessing its severity. Finding gallstones and dilation of the extrahepatic biliary tree on cross-sectional abdominal imaging further supports a diagnosis of gallstone pancreatitis. However, the reported sensitivity for detecting dilated bile ducts due to biliary obstruction varies widely, ranging from 55% to 91% across different studies. Transabdominal ultrasonography, while useful for detecting gallstones, often struggles to visualize the pancreas itself in patients with acute pancreatitis because of gas in the distended loops of the small bowel.
Table 1. Comparison of Imaging Techniques for Acute Pancreatitis
Imaging technique | Effectiveness |
---|---|
Contrast-enhanced computed tomography (CECT) | 78% sensitivity and 86% specificity for severe acute pancreatitis |
Endoscopic ultrasonography (EUS) | 100% sensitivity and 91% specificity for gallstones |
Magnetic resonance cholangiopancreatography (MRCP) | 81% to 100% sensitivity for detecting common bile duct stones; 98% negative predictive value and 94% positive predictive value for bile duct stones; As accurate as CECT in predicting severity and identifying pancreatic necrosis |
Magnetic resonance imaging (MRI) | 83% sensitivity and 91% specificity for severe acute pancreatitis |
Transabdominal ultrasonography (US) | 87% to 98% sensitivity for the detection of gallstones |
Helical computed tomography (CT) is a valuable tool for accurate imaging diagnosis and staging of pancreatitis. CT scans enable the identification of pancreatic edema, fluid collections, or cysts. They also allow for grading the severity of pancreatitis and detecting complications such as pseudocysts, abscesses, necrosis, hemorrhage, and vascular occlusions.
The CT criteria for diagnosing pancreatic necrosis rely on identifying areas within the pancreas that lack normal glandular enhancement, which can be localized or more widespread. Balthazar and colleagues demonstrated a strong correlation between the presence and extent of pancreatic necrosis and the clinical course, including morbidity and mortality. Based on this research, a CT severity index was developed, providing a numerical grading system for radiologically assessing pancreatitis severity. This system assigns a score between 0 and 10, with higher scores correlating with increased morbidity and mortality. A score of 7-10 is associated with a 92% complication rate and a 17% mortality rate, whereas a score of 0-1 is associated with minimal to no morbidity or mortality.
Careful interpretation of CT scans is crucial, as peripancreatic fluid collections can sometimes mimic areas of necrosis. Pancreatic necrosis is best assessed on CT scans performed 48 to 72 hours after the onset of acute pancreatitis. Scans performed within the first 24 hours may yield false negatives or be inconclusive. While initial CT scans are commonly performed upon admission, a repeat scan should be considered for patients who do not show rapid clinical improvement.
CT scans can detect CBD stones, with reported sensitivities as high as 80% in some studies. However, clinical experience suggests that CT is often less sensitive than transabdominal ultrasound for detecting gallstones in the bile ducts. Contrast-enhanced CT scans are more valuable than non-contrast scans for assessing the severity of acute pancreatitis. It’s important to note that CT scans can be normal in 15% to 20% of patients with mild pancreatitis. Therefore, not all patients with acute pancreatitis require a CT scan. CT imaging is most beneficial when the diagnosis is uncertain, when severe pancreatitis is suspected, or when conservative management is not effective.
In a retrospective analysis of 76 patients undergoing endoscopic retrograde cholangiopancreatography (ERCP), Neoptolemos and colleagues developed a scoring system to predict the presence of CBD stones. This system considered factors such as bilirubin levels less than 40 μmol/L (2.5 mg/dL), gamma-glutamyl transpeptidase (γ-GT) levels less than 250 IU/L, alkaline phosphatase levels less than 225 IU/L, and age younger than 70 years. The presence of all four criteria had a positive predictive value of 93%. For severe pancreatitis patients, a bilirubin level less than 40 μmol/L had an 85% predictive value for choledocholithiasis. Subsequent studies have further analyzed preoperative predictors of choledocholithiasis. However, these studies were retrospective and have not been prospectively validated. Additionally, some statistical assumptions within these studies may limit their direct clinical applicability.
The most comprehensive analysis was likely conducted by Ohken and colleagues. They developed a predictive model after reviewing data from 465 patients, of whom 115 (25%) had confirmed CBD stones. The final model used CBD diameter, maximum serum bilirubin level, AST, and alkaline phosphatase to predict choledocholithiasis with a 76% success rate.
SCORING SYSTEMS FOR ASSESSING SEVERITY
Several scoring systems are available to predict the severity of pancreatitis, and recent research has focused on comparing their predictive accuracy.
The Ranson criteria are widely used, and a higher number of positive criteria indicates a greater predicted mortality. Patients with two or fewer Ranson criteria have a mortality rate of approximately 1%, while those with more than five criteria have a mortality rate around 40%.
Other scoring systems, such as the Glasgow (or Imrie) score, may be more accurate specifically for gallstone pancreatitis. However, both the Ranson and Glasgow systems require 48 hours for a complete assessment.
The Acute Physiology and Chronic Health Evaluation (APACHE) system, while more complex to use than Ranson or Glasgow, offers the advantage of rapid severity assessment upon admission to the ICU or other high-dependency settings. Each of these systems has its own strengths and weaknesses, but they are generally considered to be roughly equivalent in their accuracy for predicting the severity of acute pancreatitis.
Research has suggested some advantages of the CT severity index in predicting the severity of acute pancreatitis compared to other scoring systems. One study found that a CT Severity Index score of five or greater correlated with longer hospital stays and increased rates of mortality and morbidity. A CT severity index score of five or more was associated with a mortality rate 15 times higher than that of patients with a score less than five. In contrast, no significant association was found between Ranson’s criteria or APACHE II scale scores and mortality or length of hospitalization in this study.
Magnetic resonance cholangiopancreatography (MRCP), a non-invasive imaging technique, is a highly effective alternative to ERCP for diagnosing choledocholithiasis. Studies have shown MRCP to be as accurate as contrast-enhanced CT in predicting pancreatitis severity and identifying pancreatic necrosis. Unlike ERCP, MRCP is not a therapeutic procedure and does not allow for stone extraction, stent placement, or biopsy. MRCP is less sensitive for detecting small stones (smaller than 4 mm), small lesions in the ampulla of Vater, and ductal strictures. However, MRCP is excellent for assessing pancreatic and peripancreatic cysts. It is particularly helpful for patients when ERCP is not feasible or unsuccessful.
The Agency for Healthcare Research and Quality (AHRQ) reviewed nine studies evaluating MRCP performance using ERCP as the reference standard. Seven of these studies demonstrated high agreement between MRCP and ERCP, with both sensitivity and specificity exceeding 90%. The review concluded that while these studies showed good concordance, the evidence did not definitively indicate which test is superior. Interestingly, Sugiyama and colleagues analyzed MRCP sensitivity based on stone size, finding lower sensitivity for stones smaller than one centimeter. This is a crucial consideration, as most stones causing pancreatitis are likely to be small.
Another advanced diagnostic technology is endoscopic ultrasonography (EUS). EUS is highly accurate in detecting stones and tumors but is used less frequently than ERCP in the initial diagnosis of biliary pancreatitis. EUS is particularly useful in obese patients and patients with ileus. It can also help determine which patients with acute pancreatitis would benefit most from therapeutic ERCP. EUS can also assist in endoscopic transmural drainage of cysts and abscesses. Both EUS and MRCP offer promising advancements in expanding the diagnostic options for identifying the cause of acute pancreatitis.
SEROLOGICAL MARKERS IN DIAGNOSIS AND PROGNOSIS
As the role of the inflammatory response and oxidative stress in the development of acute pancreatitis becomes clearer, inflammatory markers are increasingly being investigated as potential predictors of disease severity. Among the most promising markers are C-reactive protein (CRP), interleukin-6 (IL-6), and, in urine, albumin, immunoglobulin, and trypsinogen activation peptide.
Polymorphonuclear leukocyte elastase levels are significantly elevated in severe pancreatitis compared to mild cases. However, this test is not widely available and therefore has limited clinical utility in routine biliary pancreatitis diagnosis and prognosis.
Manes and colleagues evaluated the clinical value of serum interleukin-6 in comparison to C-reactive protein in a prospective study. The aim was to differentiate between necrotizing and edematous acute pancreatitis caused by common bile duct stones in the early hours of the disease. C-reactive protein showed limited effectiveness in detecting necrotizing forms of pancreatitis. The study concluded that serum interleukin-6 is a highly reliable marker for necrosis in the first 48 hours of acute biliary pancreatitis. This early identification of necrosis can be crucial for guiding timely and appropriate interventions.
TREATMENT STRATEGIES FOR ACUTE PANCREATITIS
The initial treatment for gallstone pancreatitis is typically conservative, involving bowel rest (NPO) and intravenous fluid resuscitation. Adequate fluid resuscitation is critical but is often either insufficient or overlooked in the early management of acute pancreatitis.
A British research group conducted the first prospective evaluation of ERCP’s role in acute biliary pancreatitis. In their study, 121 patients with acute pancreatitis and ultrasound evidence of gallstones were randomly assigned to either conventional medical management or urgent ERCP within 72 hours. Patients were categorized by disease severity, with half of those randomized to ERCP having severe pancreatitis. CBD stones were found in 63% of patients with severe pancreatitis but only in 25% of those with mild pancreatitis. Sphincterotomy, a procedure to widen the bile duct opening, was performed in patients with bile duct stones. In the group receiving ERCP and sphincterotomy, there was a significant reduction in complications among those with severe disease: 24% with 4% mortality compared to 61% with 18% mortality in the conservatively managed group. However, no significant difference in outcomes was observed for patients with mild pancreatitis.
This finding suggested that many patients with mild biliary pancreatitis were undergoing an invasive procedure (ERCP) unnecessarily, as they often spontaneously pass the obstructing bile duct stone.
To improve the targeted use of ERCP, various predictive scoring systems have been developed to identify patients most likely to benefit. While some critics suggest that the observed benefits of urgent ERCP were solely due to the relief of cholangitis (bile duct infection), even when cholangitis is excluded, a statistically significant benefit for patients with predicted severe acute pancreatitis can still be demonstrated.
A second single-center randomized controlled trial on endoscopic therapy for gallstone pancreatitis was published in 1993 by Fan and colleagues. This study aimed to determine if early ERCP (within 24 hours of admission) with biliary stone extraction would improve outcomes in gallstone pancreatitis compared to a conservative approach. 195 patients were randomized into two groups: early ERCP or conservative management.
Patients in the conservative treatment group only underwent ERCP and endoscopic stent (ES) placement if their clinical condition worsened. Complications were classified as local (pancreatic abscess, pseudocyst, phlegmon, pseudoaneurysm), systemic (renal failure, respiratory failure, shock, coagulopathy), and biliary (sepsis requiring surgical or endoscopic intervention).
Disease severity was predicted based on plasma glucose and urea levels at admission and the Ranson’s multifactorial scoring system applied at 48 hours. A total of 127 patients were found to have bile duct stones. Of the 97 patients undergoing urgent ERCP, 37 (38%) had stones impacted at the ampulla or in the common bile duct. All of these patients underwent successful papillotomy (widening of the ampulla) and stone extraction. ERCP failed in 10 patients, one of whom was later found to have a biliary stone. Five patients died, all of whom had predicted severe pancreatitis.
In the 98 patients randomized to conservative treatment, 27 (28%) (nine with predicted severe pancreatitis) required ERCP within the following 12 days. ERCP failed in two of these patients. Nine patients (9%) with predicted severe pancreatitis died, and four of these had CBD stones. Complications occurred in 18% of patients randomized to early ERCP and in 29% of those assigned to conservative management (p = 0.07). Biliary sepsis was more common in the conservative treatment group (12%) compared to the early ERCP group (0%). The authors concluded that emergency ERCP with or without ES is indicated in acute pancreatitis patients, particularly those with predicted severe disease.
While this study did not demonstrate a statistically significant increase in overall survival or reduction in complications following early ERCP, it did show a notable reduction in the risk of cholangitis. The study has been criticized for the high prevalence of gallstones in the Hong Kong population studied, potentially limiting the generalizability of the results to Western populations. However, careful review of the data helps in understanding the influence of disease severity, presence of cholangitis, and abnormal liver function tests on outcomes.
Despite these criticisms, the study confirmed that in experienced hands, urgent ERCP for selected patients with biliary pancreatitis is safe and beneficial, especially in reducing biliary sepsis.
A third prospective, randomized controlled trial conducted in Poland was presented in abstract form in 1995. This study involved 280 patients. 75 patients underwent early endoscopic sphincterotomy because they had a stone impacted at the ampulla of Vater. The remaining 205 patients, who did not have a visibly impacted stone, were randomized to either immediate endoscopic sphincterotomy or conservative management. The patient groups were comparable in terms of predicted pancreatitis severity, age, and gender. Combining data from all patients who received early endoscopic sphincterotomy, 17% experienced pancreatitis complications, compared to 36% in the conservative therapy group.
Mortality was significantly higher in the conservative management group (13% vs. 2%). In contrast to the previous two studies, the benefits observed in the Polish study were consistent for both predicted mild and predicted severe pancreatitis. Even more impressive results were seen when the time between the onset of gallstone pancreatitis and endoscopic sphincterotomy was less than 24 hours, with a mortality rate of 0% and complications in only 7%.
The authors concluded that early endoscopic sphincterotomy should be considered in all patients with gallstone pancreatitis (both predicted mild and severe) as it reduced both morbidity and mortality. However, this study has limitations, including the lack of full publication in a peer-reviewed journal, potential issues with true randomization, and the possibility that some patients without impacted stones might have had more severe, irreversible pancreatic damage or pancreatitis from causes other than gallstones.
Despite these limitations, the results are consistent with previous studies, suggesting that early ERCP is beneficial in a subset of patients with gallstone pancreatitis. The key difference in this study was the observed benefit in all patient groups (mild and severe), whereas previous studies primarily showed benefit in select groups, such as those with biliary sepsis or predicted severe pancreatitis.
The most debated study is the German multicenter trial by Folsch and colleagues, which randomized 238 patients with suspected biliary pancreatitis to either early ERCP within 72 hours of presentation or conservative management. Patients with jaundice were excluded. In the ERCP group, 58 of 121 patients were found to have bile duct stones. In the conservative management group, 13 of 112 patients crossed over to ERCP due to suspected bile duct stones. This study found no improvement in outcomes with early sphincterotomy. Paradoxically, there appeared to be more severe complications, including respiratory failure, in the early ERCP group, and a numerically higher mortality rate.
The authors concluded that early ERCP was not indicated for patients with gallstone pancreatitis who did not have evidence of biliary obstruction. This study has faced several criticisms. First, the exclusion of patients with obstructive jaundice (bilirubin > 5.0 mg/dL) biased the study towards the conservative treatment group, as these patients were more likely to have CBD stones and benefit from biliary decompression. Second, unlike prior studies from single centers with experienced endoscopists, the Folsch study included patients from 22 centers, some contributing as few as two patients per year. This raises concerns about the experience and expertise of endoscopists performing urgent ERCPs in lower-volume centers. Third, the statistically significant increase in respiratory failure in the early ERCP group was not observed in previous studies. The lack of detailed data on the nature of respiratory problems, comorbidities, and their relation to predicted pancreatitis severity in the published paper makes this finding difficult to interpret. Fourthly, the early termination of the Folsch study reduced its statistical power to definitively conclude that early ERCP with endoscopic sphincterotomy is not beneficial in specific subgroups of gallstone pancreatitis patients.
Unless there is strong clinical evidence of a persistent bile duct stone, such as rising serum bilirubin or clear imaging evidence of an intraductal stone, routine ERCP is generally unnecessary and introduces avoidable risks for patients with mild to moderate biliary pancreatitis who are scheduled for cholecystectomy. For most patients with suspected biliary pancreatitis, bile duct stones have likely passed by the time cholangiography (bile duct imaging) is performed. In these cases, ERCP can be deferred. Any remaining ductal stones can be identified during intraoperative cholangiography performed during laparoscopic cholecystectomy. These stones can then be removed either postoperatively or even intraoperatively via ERCP. In specialized centers with expertise, laparoscopic common bile duct exploration can also be performed. If ERCP is unsuccessful, patients can be referred to tertiary endoscopy centers where biliary access is almost always achievable.
UK guidelines for gallstone pancreatitis recommend definitive treatment, including cholecystectomy, during the initial hospital admission or within two weeks of discharge. However, achieving this target is not always feasible. A study by Sanjay and colleagues (2008) reviewed the current management of gallstone pancreatitis in a university hospital and assessed the risk associated with interval cholecystectomy (cholecystectomy performed after the initial admission). This study showed that overall, 62% of patients with gallstone pancreatitis receive definitive therapy during the index admission. However, surgery was often delayed in patients with severe gallstone pancreatitis, and 19 out of 30 of these patients underwent endoscopic sphincterotomy before discharge. The study concluded that endoscopic sphincterotomy and interval cholecystectomy in severe gallstone pancreatitis is associated with minimal morbidity and readmission rates, making it a reasonable alternative to index cholecystectomy in patients with severe disease.
ERCP is appropriate for post-cholecystectomy patients with suspected biliary pancreatitis. However, in many of these cases, the etiology may be non-biliary stone related, such as sphincter of Oddi dysfunction. In these situations, conventional diagnostic and therapeutic ERCP techniques can be particularly risky, and protective measures like pancreatic stent placement may be advisable.
Recurrent biliary pancreatitis in patients with moderately severe gallstone pancreatitis is rare after ERCP and endoscopic sphincterotomy. Discharging these patients after ERCP allows for interval laparoscopic cholecystectomy, but close follow-up is essential due to the potential severity of their underlying condition.
Laparoscopic cholecystectomy with preoperative endoscopic CBD clearance is generally recommended as the treatment of choice for biliary acute pancreatitis. In mild cases, cholecystectomy can be safely performed within seven days. In severe cases, particularly with extensive pancreatic necrosis, it is advisable to wait at least three weeks before cholecystectomy due to an increased risk of infection.
According to Chang and colleagues, for patients with mild to moderate gallstone pancreatitis without cholangitis, selective postoperative ERCP and CBD stone extraction are associated with shorter hospital stays, lower costs, no increase in combined treatment failure rates, and a significant reduction in ERCP use compared to routine preoperative ERCP. However, this study was limited by its small sample size.
The optimal timing of cholecystectomy following ERCP for biliary pancreatitis varies significantly based on the severity of pancreatitis and the patient’s overall health. Cholecystectomy often follows several weeks after necrotizing pancreatitis has resolved. The risk of recurrent biliary pancreatitis is expected to be quite low if endoscopic sphincterotomy is performed during the ERCP. There is broad consensus that laparoscopic cholecystectomy should be performed after endoscopic sphincterotomy for gallstone pancreatitis if the patient is a suitable surgical candidate.
Patients with biliary pancreatitis that resolves quickly should ideally undergo cholecystectomy before being discharged from the initial hospitalization to prevent recurrence.
CONCLUSIONS
Mild biliary pancreatitis can typically be managed conservatively, and only a small subset of these patients will require urgent ERCP. If there is concern about a retained common bile duct stone, ERCP can be safely and effectively performed after laparoscopic cholecystectomy. The timing of cholecystectomy after ERCP for biliary pancreatitis is highly dependent on the severity of the pancreatitis. Patients with severe pancreatitis and those with ascending cholangitis are more likely to benefit from early ERCP and endoscopic sphincterotomy to decompress the biliary system. Cholecystectomy may be delayed until several weeks after necrotizing pancreatitis has resolved. The risk of recurrent biliary pancreatitis is significantly reduced if endoscopic sphincterotomy is performed during the ERCP.
There is increasing recognition of the pivotal role of inflammatory mediators, such as interleukins and TNF-α, in the development of clinical pancreatitis. Serum interleukin-6 is a reliable early marker of necrosis in acute biliary pancreatitis. In centers with experienced endoscopists, the complication rate of ERCP, even in acutely ill patients, appears to be low.
However, the expertise available at large academic centers with high procedural volumes may not be representative of smaller community hospitals. This underscores the importance for community gastroenterologists to carefully select patients for urgent ERCP based on clear indications and risk-benefit assessment in biliary pancreatitis diagnosis and management.
MRCP is as accurate as contrast-enhanced CT for predicting pancreatitis severity and identifying pancreatic necrosis but is less sensitive for detecting small stones. Endoscopic ultrasonography is valuable in obese patients and those with ileus and can help determine which patients with acute pancreatitis would benefit most from therapeutic ERCP, further refining the diagnostic and treatment pathways for biliary pancreatitis.
Footnotes
Source of Support: Nil
Conflict of Interest: None declared.
REFERENCES
(References are identical to the original article and thus not repeated here for brevity, as per instructions.)